Objective—To determine the efficacy of trilostane, a
3β-hydroxysteroid dehydrogenase inhibitor, in dogs
with pituitary-dependent hyperadrenocorticism (PDH).
Animals—11 dogs with PDH.
Procedure—The initial dose of trilostane was 30 mg,
PO, q 24 h for dogs that weighed < 5 kg and 60 mg,
PO, q 24 h for dogs that weighed ≥ 5 kg. A CBC
count, serum biochemical analyses, urinalysis, ACTH
stimulation test, and ultrasonographic evaluation of
the adrenal glands were performed in each dog 1, 3
to 4, 6 to 7, 12 to 16, and 24 to 28 weeks after initiation
Results—All dogs responded well to treatment. All had
reductions in polyuria-polydipsia and panting and an
increase in activity. Polyphagia decreased in 9 of 10
dogs, and 9 of 11 dogs had improvement of coat quality
and skin condition. Concentration of cortisol after
ACTH stimulation significantly decreased by 1 week
after initiation of treatment. After treatment for 6
months, clinical signs resolved in 9 dogs. In the other 2
dogs, marked clinical improvement was reported for 1
dog, and moderate improvement was reported in the
other dog. Ultrasonographically, there was a considerable
change in the parenchyma and an increase in size
of the adrenal glands. Adverse effects consisted of 1
dog with transient lethargy and 1 dog with anorexia.
Conclusions and Clinical Relevance—Trilostane is
an efficacious and safe medication for treatment of
dogs with PDH. Additional studies in a larger group of
dogs and characterization of progressive changes in
adrenal glands are needed. (Am J Vet Res 2002;63:506–512).
Objective—To compare serum concentrations of
1,25-dihydroxycholecalciferol (1,25-[OH]2D3) and
25-hydroxycholecalciferol (25-[OH]D3) in healthy
control dogs and dogs with naturally occurring
acute renal failure (ARF) and chronic renal failure
Animals—24 control dogs, 10 dogs with ARF, and 40
dogs with CRF.
Procedure—Serum concentrations of 1,25-(OH)2D3
were measured by use of a quantitative radioimmunoassay,
and serum concentrations of 25-
(OH)D3 were measured by use of a protein-binding
Results—Mean ± SD serum concentration of 1,25-
(OH)2D3 was 153 ± 50 pmol/L in control dogs, 75 ± 25
pmol/L in dogs with ARF, and 93 ± 67 pmol/L in dogs
with CRF. The concentration of 1,25-(OH)2D3 did not
differ significantly between dogs with ARF and those
with CRF and was in the reference range in most
dogs; however, the concentration was significantly
lower in dogs with ARF or CRF, compared with the
concentration in control dogs. Mean ± SD concentration
of 25-(OH)D3 was 267 ± 97 nmol/L in control
dogs, 130 ± 82 nmol/L in dogs with ARF, and 84 ± 60
nmol/L in dogs with CRF. The concentration of 25-
(OH)D3 was significantly lower in dogs with ARF or
CRF, compared with the concentration in control
Conclusions and Clinical Relevance—The concentration
of 1,25-(OH)2D3 was within the reference
range in most dogs with renal failure. Increased
serum concentrations of parathyroid hormone indicated
a relative deficiency of 1,25-(OH)2D3. A
decrease in the serum concentration of 25-(OH)D3 in
dogs with CRF appeared to be attributable to
reduced intake and increased urinary loss. (Am J Vet Res 2003;64:1161–1166)
Objective—To evaluate owner compliance with longterm
home monitoring of blood glucose concentrations
in diabetic cats and assess the influence of
home monitoring on the frequency of reevaluation of
those cats at a veterinary hospital.
Animals—26 cats with diabetes mellitus.
Procedure—Medical records of diabetic cats for
which home monitoring was undertaken were
reviewed, and owners were contacted by telephone.
Signalment, laboratory test results, insulin treatment
regimen, details of home monitoring, clinical signs
during treatment, frequency of follow-up examinations,
and survival times were evaluated.
Results—Monitoring of cats commenced within 12
weeks (median, 3 weeks) after initial evaluation; 8
owners were unable to perform home monitoring,
and 1 cat was euthanatized after 1 week. In 17 cats,
duration of home monitoring was 4.8 to 46.0 months
(median, 22.0 months); 6 cats died after 7.0 to 18.0
months (median, 13.0 months). In 11 cats, home
monitoring was ongoing at completion of the study
(12.0 to 46.0 months' duration). Fourteen owners
completed blood glucose curves every 2 to 4 weeks.
Cats managed with home monitoring received higher
dosages of insulin, compared with cats that were not
monitored. Four of 17 cats managed by home monitoring
had transient resolution of diabetes mellitus for
as long as 1 year. Home monitoring did not affect the
frequency of reevaluation at the veterinary hospital.
Conclusions and Clinical Relevance—Owner compliance
with long-term home monitoring appeared to
be satisfactory, and home monitoring did not affect
the frequency of reevaluation of patients by veterinarians.
(J Am Vet Med Assoc 2004;225:261–266)
Objective—To evaluate the effect of trilostane on
serum concentrations of aldosterone, cortisol, and
potassium in dogs with pituitary-dependent hyperadrenocorticism
(PDH), compare the degree of reduction
of aldosterone with that of cortisol, and compare
aldosterone concentrations of healthy dogs with
those of dogs with PDH.
Animals—17 dogs with PDH and 12 healthy dogs.
Procedure—For dogs with PDH, the initial dose of
trilostane was selected in accordance with body
weight. A CBC count, serum biochemical analyses,
and ACTH stimulation tests were performed in each
dog. Dogs were evaluated 1, 3 to 4, 6 to 8, and 10 to
12 weeks after initiation of treatment. Healthy dogs
were evaluated only once.
Results—Serum aldosterone concentrations before
ACTH stimulation did not change significantly after initiation
of treatment with trilostane. At each evaluation
after initiation of treatment, serum aldosterone concentrations
after ACTH stimulation were significantly
lower than corresponding concentrations before initiation
of treatment. The overall effect of trilostane on
serum aldosterone concentration was less pronounced
than the effect on serum cortisol concentration.
Median potassium concentrations increased
slightly after initiation of treatment with trilostane.
Dogs with PDH had significantly higher serum aldo
sterone concentrations before and after ACTH stimulation
than healthy dogs.
Conclusions and Clinical Relevance—Treatment
with trilostane resulted in a reduction in serum cortisol
and aldosterone concentrations in dogs with PDH,
although the decrease for serum aldosterone concentration
was smaller than that for serum cortisol concentration.
There was no correlation between serum
concentrations of aldosterone and potassium during
treatment. (Am J Vet Res 2004;65:1245–1250)
Objective—To evaluate the use of high-resolution manometry (HRM) in awake and sedated dogs and to assess potential effects of a standard sedation protocol.
Procedures—An HRM catheter with 36 pressure sensors was inserted intranasally in each dog. After an adaption period of 5 minutes, each set of measurements included 5 swallows of a liquid and 5 swallows of a solid bolus. Measurements were repeated 30 minutes after IM administration of buprenorphine and acepromazine.
Results—HRM was successfully performed in 14 dogs. Data sets of 8 dogs were adequate for analysis. For the upper esophageal sphincter, median values of baseline pressure, residual pressure, relaxation time to nadir, and relaxation duration were determined for awake and sedated dogs for liquid and solid swallows. For the tubular portion of the esophagus, median values of peristaltic contractile integral, bolus transit time, and contractile front velocity were determined for awake and sedated dogs for liquid and solid swallows. For the lower esophageal sphincter, median values of baseline pressure and residual pressure were determined for awake and sedated dogs for liquid and solid swallows. Significant differences (awake vs sedated) were found for the upper esophageal sphincter residual pressure (liquid swallows), relaxation time to nadir (liquid swallows), bolus transit time (solid swallows), and contractile front velocity (solid swallows).
Conclusions and Clinical Relevance—HRM was feasible for evaluation of esophageal function in most awake dogs. Although sedation in uncooperative patients may minimally influence results of some variables, an overall assessment of swallowing should be possible.
OBJECTIVE To evaluate the effects of storage conditions and duration on cobalamin concentration in serum samples from dogs and cats.
SAMPLE Serum samples from 9 client-owned cats and 9 client-owned dogs.
PROCEDURES Serum harvested from freshly obtained blood samples was separated into 11 aliquots/animal. One aliquot (baseline sample) was routinely transported in light-protected tubes to the laboratory for cobalamin assay; each of the remaining aliquots was stored in a refrigerator (6°C; n = 5) or at room temperature (20°C) with exposure to daylight (5) for 24, 48, 72, 96, or 120 hours. Aliquots were subsequently wrapped in aluminum foil, frozen (−20°C), and then transported to the laboratory for measurement of cobalamin concentration, all in the same run. Percentage decrease in cobalamin concentration from baseline was analyzed by means of linear mixed modeling.
RESULTS No differences in cobalamin values were identified between cats and dogs; therefore, data for both species were analyzed together. Median baseline serum cobalamin concentration was 424 ng/L (range, 178 to 1,880 ng/L). Values for serum samples stored with daylight exposure at room temperature were significantly lower over time than were values for refrigerated samples. Although values for refrigerated samples did not decrease significantly from baseline values over time, values for the other storage condition did; however, the mean percentage decrease for serum samples stored at room temperature was small (0.14%/h; 95% confidence interval, 0.07% to 0.21%/h).
CONCLUSIONS AND CLINICAL RELEVANCE Overall, serum cobalamin concentration appeared stable for 5 days when feline and canine serum samples were refrigerated at 6°C. The effect of light and room temperature on serum cobalamin concentration, although significant, was quite small for samples stored with these exposures for the same 5-day period.
Objective—To investigate agreement of a feline pancreas–specific lipase assay and a colorimetric lipase assay with a 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) substrate with results of pancreatic ultrasonography in cats with suspicion of pancreatitis.
Design—Retrospective case series.
Animals—161 client-owned cats with suspicion of pancreatitis.
Procedures—Feline pancreas–specific lipase concentration and DGGR lipase activity were measured from the same blood sample in cats undergoing investigation for pancreatitis, with < 24 hours between ultrasonography and lipase determinations. Ultrasonographic variables evaluated were ultrasonographic diagnosis of pancreatitis, enlargement, margins, echogenicity, mesenteric echogenicity, peripancreatic free fluid, cysts, masses, and common bile and pancreatic duct dilation. Agreement was assessed by use of the Cohen κ coefficient.
Results—Agreement between the lipase assays was substantial (κ = 0.703). An ultrasonographic diagnosis of pancreatitis had fair agreement with feline pancreas–specific lipase concentration > 5.4 μg/L (κ = 0.264) and DGGR lipase activity > 26 U/L (κ = 0.221). The greatest agreement between feline pancreas–specific lipase concentration > 5.4 μg/L and DGGR lipase activity > 26 U/L was found for a hypoechoic and mixed-echoic (κ = 0.270 and 0.266, respectively), hypoechoic (κ = 0.261 and 0.181, respectively), and enlarged (κ = 0.218 and 0.223, respectively) pancreas.
Conclusions and Clinical Relevance—Agreement between pancreatic ultrasonography and lipase assay results was only fair. It remains unknown whether lipase results or pancreatic ultrasonography constitutes the more accurate test for diagnosing pancreatitis; therefore, results of both tests need to be interpreted with caution.
Objective—To evaluate day-to-day variability in blood glucose curves (BGCs) generated at home and at the clinic for cats with diabetes mellitus.
Animals—7 cats with diabetes mellitus.
Procedures—BGCs generated at home on 2 consecutive days and within 1 week at the clinic were obtained twice. On each occasion, insulin dose, amount of food, and type of food were consistent for all 3 BGCs. Results of curves generated at home were compared with each other and with the corresponding clinic curve.
Results—Differences between blood glucose concentration determined after food was withheld (fasting), nadir concentration, time to nadir concentration, maximum concentration, and mean concentration during 12 hours had high coefficients of variation, as did the difference between fasting blood glucose and nadir concentrations and area under the curve of home curves. Differences between home curve variables were not smaller than those between home and clinic curves, indicating large day-to-day variability in both home and clinic curves. Evaluation of the paired home curves led to the same theoretical recommendation for adjustment of insulin dose on 6 of 14 occasions, and evaluation of home and clinic curves resulted in the same recommendation on 14 of 28 occasions. Four of the 6 paired home curves in cats with good glycemic control and 2 of the 8 paired home curves in cats with poor glycemic control led to the same recommendation.
Conclusions and Clinical Relevance—Considerable day-to-day variability was detected in BGCs generated at home. Cats with good glycemic control may have more reproducible curves generated during blood collection at home than cats with poorer control.
Objective—To evaluate the effects of cisapride and metoclopramide hydrochloride administered orally on the lower esophageal sphincter (LES) resting pressure in awake healthy dogs.
Animals—6 adult Beagles.
Procedures—Each dog was evaluated after administration of a single dose of cisapride (0.5 mg/kg), metoclopramide (0.5 mg/kg), or placebo (empty gelatin-free capsule) in 3 experiments performed at 3-week intervals. To measure LES pressure, a high-resolution manometry catheter equipped with 40 pressure sensors spaced 10 mm apart was used. For each experiment, LES pressure was recorded during a 20-minute period with a virtual electronic sleeve emulation before treatment (baseline) and at 1, 4, and 7 hours after drug or placebo administration. A linear mixed-effects model was used to test whether the 3 treatments affected LES pressure differently.
Results—In the cisapride, metoclopramide, and placebo experiments, median baseline LES pressures were 29.1, 30.5, and 29.0 mm Hg, respectively. For the cisapride, metoclopramide, and placebo treatments, median LES pressures at 1 hour after administration were 44.4, 37.8, and 36.6 mm Hg, respectively; median LES pressures at 4 hours after administration were 50.7, 30.6, and 31.1 mm Hg, respectively; and median LES pressures at 7 hours after administration were 44.3, 28.5, and 33.3 mm Hg, respectively. The LES pressures differed significantly only between the placebo and cisapride treatments.
Conclusions and Clinical Relevance—Results suggested that orally administered cisapride may be of benefit in canine patients for which an increase in LES pressure is desirable, whereas orally administered metoclopramide did not affect LES resting pressures in dogs.
Objective—To evaluate whether determination of
parathyroid gland size by use of ultrasonography is
helpful in differentiating acute renal failure (ARF) from
chronic renal failure (CRF) in dogs.
Animals—20 dogs with renal failure in which serum
creatinine concentration was at least 5 times the
upper reference limit. Seven dogs had ARF, and 13
dogs had CRF. Twenty-three healthy dogs were used
Procedure—Dogs were positioned in dorsal recumbency
for ultrasonographic examination of the ventral
portion of the neck, A 10-MHz linear-array high-resolution
transducer was used. The size of the parathyroid
gland was determined by measuring the maximal
length of the gland on the screen when it was imaged
in longitudinal section. For comparison among
groups, the longest linear dimension of any of the
parathyroid glands of each dog was used.
Results—Size of the parathyroid glands in the control
dogs varied from 2.0 to 4.6 mm (median, 3.3 mm). In the
dogs with ARF, gland size ranged from 2.4 to 4.0 mm
(median, 2.7), which was not significantly different from
controls. In dogs with CRF, the glands were more distinctly
demarcated from the surrounding thyroid tissue,
than those of controls and dogs with ARF. Sizes ranged
from 3.9 to 8.1 mm (median, 5.7 mm), which was significantly
larger, compared with controls and dogs with
Conclusion and Clinical Relevance—In dogs with
severe azotemia, ultrasonographic examination of the
parathyroid glands was helpful in differentiating ARF
from CRF. Size of the parathyroid glands appeared to
be related to body weight. (J Am Vet Med Assoc